J H Bae1, T-G Kwon, D-W Hyun, C S Rihal, A Lerman. 1. Division of Cardiology, College of Medicine, Konyang University Hospital, Seo-gu, Daejeon, South Korea. janghobae@yahoo.co.kr
Abstract
OBJECTIVES: Slow flow phenomenon is a serious complication of percutaneous coronary intervention (PCI) and is associated with a poor prognosis. We sought to evaluate the characteristics of lesions predisposing to the slow/no-reflow phenomenon during primary PCI in patients with acute myocardial infarction. METHODS: The study subjects consisted of 57 consecutive patients (mean age 58.5 (SD 14.5) years, 45 males) who underwent primary PCI for acute myocardial infarction and intravascular ultrasound-virtual histology (IVUS-VH) examination. Slow flow was defined as <or= thrombolysis in myocardial infarction grade 2 after PCI. RESULTS: Slow flow developed in 12 patients (eight males). Patients with slow flow were likely to be older (67.5 (13.8) years vs 56.2 (13.9) years, p = 0.015), had more cardiogenic shock (16.7% vs 2.2%, p = 0.046), larger fibrofatty volume over the entire lesion length (36.7 (25.5) mm(3) vs 18.0 (18.6) mm(3), p = 0.006), higher remodelling index (1.10 (0.17) vs 0.99 (0.16), p = 0.043), larger plaque area (16.2 (5.4) mm(2) vs 12.5 (4.9) mm(2), p = 0.025), fibrous area (8.0 (3.3) mm(2) vs 5.4 (3.0) mm(2), p = 0.014) and fibrofatty area (2.7 (2.2) mm(2) vs 1.3 (1.6) mm(2), p = 0.016) at the minimal lumen site than those without slow flow (37 males). Multivariate analysis revealed that the fibrofatty volume over the entire lesion length was the only independent factor (beta = 0.359, 95% confidence interval 0.002 to 0.012, p = 0.006) for slow flow during primary PCI. CONCLUSIONS: This study suggests that slow flow may be dependent on the tissue characterisation (fibrofatty volume) of the underlying lesion at the time of the primary PCI for acute myocardial infarction.
OBJECTIVES: Slow flow phenomenon is a serious complication of percutaneous coronary intervention (PCI) and is associated with a poor prognosis. We sought to evaluate the characteristics of lesions predisposing to the slow/no-reflow phenomenon during primary PCI in patients with acute myocardial infarction. METHODS: The study subjects consisted of 57 consecutive patients (mean age 58.5 (SD 14.5) years, 45 males) who underwent primary PCI for acute myocardial infarction and intravascular ultrasound-virtual histology (IVUS-VH) examination. Slow flow was defined as <or= thrombolysis in myocardial infarction grade 2 after PCI. RESULTS: Slow flow developed in 12 patients (eight males). Patients with slow flow were likely to be older (67.5 (13.8) years vs 56.2 (13.9) years, p = 0.015), had more cardiogenic shock (16.7% vs 2.2%, p = 0.046), larger fibrofatty volume over the entire lesion length (36.7 (25.5) mm(3) vs 18.0 (18.6) mm(3), p = 0.006), higher remodelling index (1.10 (0.17) vs 0.99 (0.16), p = 0.043), larger plaque area (16.2 (5.4) mm(2) vs 12.5 (4.9) mm(2), p = 0.025), fibrous area (8.0 (3.3) mm(2) vs 5.4 (3.0) mm(2), p = 0.014) and fibrofatty area (2.7 (2.2) mm(2) vs 1.3 (1.6) mm(2), p = 0.016) at the minimal lumen site than those without slow flow (37 males). Multivariate analysis revealed that the fibrofatty volume over the entire lesion length was the only independent factor (beta = 0.359, 95% confidence interval 0.002 to 0.012, p = 0.006) for slow flow during primary PCI. CONCLUSIONS: This study suggests that slow flow may be dependent on the tissue characterisation (fibrofatty volume) of the underlying lesion at the time of the primary PCI for acute myocardial infarction.
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